Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004153 (atherosclerosis)
77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Magnesium deficiency may play a role in the pathogenesis of atherosclerosis, cardiac arrhythmias, and coronary spasm. Because less than 1% of magnesium (Mg) is extracellular, the serum magnesium (sMg) does not always accurately reflect intracellular Mg stores. To determine the frequency of Mg deficiency in patients with cardiovascular disease, we measured blood mononuclear cell Mg content (mMg) and sMg concentrations in 104 unselected patients admitted to our intensive cardiac care unit (CCU). Twenty-seven normal healthy controls and 33 hypomagnesemic patients with chronic alcoholism and/or malabsorption syndrome served as reference groups. The sMg concentration in the CCU patients was 2.05 +/- 0.03 mg/dl (mean +/- SEM), and did not differ from normal controls (mean 2.01 +/- 0.03 mg/dl). Only 8 of 104 CCU patients were hypomagnesemic (7.7%). mMg in the CCU patients, however, was significantly lower than in the normal controls (1.15 +/- 0.02 micrograms/mg protein and 1.34 +/- 0.02 micrograms/mg protein respectively, p less than 0.001). Fifty-three percent (55 of 104) of CCU patients had mMg contents less than 1.119 micrograms/mg protein, i.e., below that of the lowest normal control. mMg was significantly lower in those patients with congestive heart failure (mMg = 1.08 +/- 0.03 micrograms/mg protein) when compared to those patients without congestive heart failure (1.23 +/- 0.02 micrograms/mg protein, p less than 0.001). We conclude that the incidence of intracellular Mg deficiency in patients with cardiovascular disease is much higher than the sMg would lead one to suspect, and may contribute to clinical cardiovascular morbidity.
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PMID:Low blood mononuclear cell magnesium in intensive cardiac care unit patients. 395 55

Endothelia lining the 2 surfaces (arterial and ventricular) of the posterior cusp of aortic valves from normocholesterolemic, New Zealand white rabbits were found to display pleomorphic surface features characterized by differences in cellular shape and orientation to the direction of blood flow, microappendage populations (microvilli and blebs), nuclear contours and the surface reactions of cationic dyes (RR, AB) and peroxidase-conjugated lectins (Con A, Limulin, WGA). With the aid of SEM and TEM, the cells lining the arterial surfaces appeared relatively smooth and flattened with a moderate to heavy reaction of the carbohydrate cell coat at the blood interface. By contrast, the contours of the endothelia lining the ventricular surfaces were noticeably raised with numerous plasmalemmal microappendages and only a moderate dye/lectin reaction. Observations of similar endothelial populations from diet-induced, hypercholesterolemic rabbits (500 mg/dl) revealed a variety of dramatic changes in the cells lining the arterial surfaces of the valvular cusps. No severe changes were observed in the endothelia of the ventricular surfaces. Such findings are suggestive further of the importance of the interaction between the environment and the endothelial cell coat as influencing factors in the onset of intramural lipid infiltration.
Atherosclerosis 1985 Mar
PMID:Surface responses of aortic valve endothelia from diet-induced, hypercholesterolemic rabbits. 399 84

Verapamil and other slow channel calcium antagonists have been reported to retard atherosclerosis in rabbits fed a high cholesterol diet. Because atherosclerosis in such a model may differ significantly from human atherosclerosis, experiments were conducted to prevent atherosclerosis with verapamil in the Watanabe heritable hyperlipidemic (WHHL) rabbit, which is a genetic, metabolic and pathologic model of homozygous familial hypercholesterolemia. At 2 months of age, 23 WHHL rabbits were divided into two groups since earlier studies showed no macroscopic atherosclerosis at 2 months. Group A (n = 11) was fed standard rabbit chow for 6 months. Group B (n = 12) received oral verapamil (46 mg/kg per day) absorbed in the identical chow as fed to Group A and subcutaneous verapamil (0.25 mg/kg twice daily 6 days a week). In Group B, mean serum verapamil concentrations (+/- SEM) averaged 16.9 +/- 1.9 ng/ml at 3 hours after subcutaneous injection. Sex ratios and serum cholesterol concentrations were the same in both groups. The percent of aortic surface area with visible plaque in Group A versus B was 49 +/- 7 versus 43 +/- 7%, respectively, of the entire aorta, and 61 +/- 5 versus 65 +/- 5%, respectively, of the proximal 3 cm of aorta (p = NS). Thus, verapamil did not suppress atherosclerosis in WHHL rabbits at serum drug levels greater than those reported to be effective in other models.
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PMID:Failure of a slow channel calcium antagonist, verapamil, to retard atherosclerosis in the Watanabe heritable hyperlipidemic rabbit: an animal model of familial hypercholesterolemia. 400 71

Timed pregnant (8 days) Sprague-Dawley rats were fed ground stock diet (CON) or ground stock diet with 4% cholestyramine (CTR) until day 20 of gestation. Animals in both groups gained weight equally well during the study period (CON (n = 7), 308 +/- 7 g; CTR (n = 6), 315 +/- 7 g, mean +/- SEM). At the end of the study period, plasma cholesterol in the CTR group was significantly greater than that in the control group (CON n = 7, 91 +/- 4 mg/dl; CTR (n = 6), 108 +/- 5 mg/dl, P less than 0.05). The fecal excretion of both neutral steroids and bile acids, studied for 3 days between days 15 and 18 of gestation, was significantly enhanced by CTR treatment. (Neutral steroids: CON, 3.9 +/- 0.3; CTR, 10.4 +/- 0.3, P less than 0.05. Bile acids: CON, 7.6 +/- 0.4; CTR, 25.8 +/- 1.7, P less than 0.05, mg/100 g body wt/day). Bile acid pool size, measured at day 20 of gestation, however, was not significantly different. Consistent with these results was the finding that hepatic cholesterol 7 alpha-hydroxylase activity (the rate-limiting enzyme of bile acid biosynthesis) measured at day 20 of gestation was significantly enhanced by CTR treatment (CON (n = 4), 14.7 +/- 1.7; CTR (n = 4), 34.8 +/- 3.3, pmoles/mg/min, P less than 0.05). The atypical finding of hypercholesterolemia, despite the CTR-induced enhanced turnover of cholesterol, may be due to changes in the homeostatic mechanisms of cholesterol and bile acid metabolism during pregnancy.
Atherosclerosis 1985 Nov
PMID:Cholestyramine treatment during pregnancy in the rat results in hypercholesterolemia. 408 52

The formation of craters under in vitro hypoxic conditions in the human venous endothelium was studied by scanning-(SEM) and transmission electron microscopy (TEM). Craters are a result of collapsed intracytoplasmatic vesicles which is probably due to extraction of fluid during processing. Thus craters are thought to be artefacts of preparation. This investigation indicates that fusion of caveolae is involved in intracytoplasmatic vesicle formation. A new quantitative method is described for studying endocytosis. Whole vein wall preparations immersed in isotonic saline (approximately 1 h) revealed reduced endocytotic activity in the luminal plasma membrane (LPM) of endothelial cells compared to the basal plasma membrane (BPM), where the endocytotic activity was increased.
Atherosclerosis 1985 Dec
PMID:Crater formation and endocytosis in human endothelial cells in vitro. 409 83

Endothelial injury and increased mitotic activity are early features in the pathogenesis of intimal thickening in arteries. This study examines the effect of systemic nicotine on mitotic activity in endothelial cells. Nine adult mice were given nicotine in their drinking water for 5 weeks. The dose (5 mg/kg body wt/day) was equivalent to a human smoking 50-100 cigarettes/day. A group of 8 similar mice, not exposed to nicotine, was the control. At the end of the exposure period all mice were injected with [3H]thymidine (1 microCi/g body wt) and were killed 24 h later. After perfusion fixation, en-face preparations of aortic endothelium were processed for autoradiography. In nicotine-affected endothelium 0.46 +/- 0.11% (SEM) of cells were labelled, which was significantly higher (P less than 0.01) than in controls (0.14 +/- 0.06%). However, there was no difference in cell density between the groups. On this evidence it was concluded that the rate of cell loss, or cell turnover, was greater in nicotine-affected endothelium. Because other studies have shown that increased mitotic activity and cell loss are established features of endothelial injury, the present findings provide evidence in support of the hypothesis that nicotine contributes to the pathogenesis of arterial disease in smokers.
Atherosclerosis 1985 Dec
PMID:The effect of nicotine on aortic endothelial cell turnover. An autoradiographic study. 409 85

51 chronic haemodialysis patients with hypertriglyceridaemia were given a daily oral dose of 2.4 g D,L-carnitine for 30 days to investigate a possible hypolipaemic effect. After 30 days' D,L-carnitine treatment the mean (+/- SEM) serum triglyceride concentration had decreased significantly from 3.50 +/- 0.39 to 2.87 +/- 0.27 mmol/l. Serum total cholesterol did not change. However, HDL cholesterol increased significantly from 0.89 +/- 0.05 to 1.35 +/- 0.07 mmol/l. This decrease in serum triglycerides and return of HDL cholesterol to normal levels in haemodialysis patients may be the result of correction of carnitine deficiency. Such treatment could reduce the risk factors for atherosclerosis and coronary-artery disease in uraemic patients.
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PMID:Carnitine improves lipid anomalies in haemodialysis patients. 610 51

Mammalian, cardiac endothelium has a surface topography that is characterized by plasmalemmal microappendages, nuclear bulges and ruffled cellular margins. SEM of the endothelial population over the two surfaces of the anterior cusp (leaflet) of the rabbit mitral valve revealed a very pleomorphic topography. The atrial and ventricular surfaces of the cusp displayed differences in microappendage population, cell density, nuclear contour and surface reactivity to Ruthenium Red and Concanavalin A. Comparative studies of similar populations from diet-induced hypercholesterolemic rabbits suggested an enhanced endothelial permeability as observed by an increase in cytoplasmic vesicles containing RR or Con A and by their intercellular passage into the subendothelium. Concomitant with these changes were disproportionate responses in the surface reaction of the carbohydrate cell coat (glycocalyx). The endothelial cells over the ventricular surface of the anterior cusp displayed the most dramatic changes with the appearance of numerous microappendages and intercellular fenestrations, the loss of RR and Con A surface reaction and the engorgement of the adjacent intima with foam-like cells containing the surface markers. Such surface responses appeared to precede or accompany alterations in endothelial integrity which suggests the importance of the blood-endothelial interface in the maintenance of the vascular wall.
Atherosclerosis 1982 Nov
PMID:Surface topography of mitral valve endothelium from diet-induced, hypercholesterolemic rabbits. 618 63

The NaOH sonication digestion technique permits rapid isolation and exposure of intact networks of elastic fibers in vascular tissue for 3-dimensional observation with the SEM. The configuration of the network of elastic fibers within the vascular wall of large elastic arteries (aorta) is generally agreed to be a flexible framework through which smooth muscle cells and collagenous fibers are interwoven. However, the configuration of elastic fiber networks in muscular arteries, medium sized veins and smaller vessels remains unknown. When the lengthy standard biochemical elastin purification techniques were applied to vessels containing lesser amounts of elastic tissue and finer elastic fibers, the vessels were completely digested. In contrast, the digestion and sonication technique isolated and exposed intact networks of delicate elastic fibers in blood vessels which do not contain large amounts of elastic tissue. Unfixed vessels were cut into short segments, placed in 0.5 N NaOH and sonicated for 20-40 min. The specimens were rinsed in deionized distilled H2O, then autoclaved for 30 min. The tissue was rinsed a second time, fixed and processed routinely for SEM. Elastic stains and enzymatic digestion with chromatographically purified elastase and collagenase confirmed that the digestion and sonication technique produced clean, isolated networks of elastic fibers. Knowledge of the configuration of the networks of elastic fibers in different vessels enhances understanding of distensibility characteristics of individual vessels and serves as a baseline for studying alterations in the elastic framework which occur during aging and disease processes such as atherosclerosis, arterial hypertension and aneurysms.
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PMID:A rapid digestive technique to expose networks of vascular elastic fibers for SEM observation. 620 43

The appearance of the aortic wall of rabbits fed a lanolin containing diet was examined by scanning (SEM) and transmission electron microscopy (TEM) in order to clarify the mechanism of removal of lipids deposited in the aorta. SEM study showed that circulating leukocytes penetrated into the arterial wall in the early phase of the experimental atherosclerosis. In some specimens, spherical bodies with a diameter of 10-30 mu were observed along the cleavage of the marginal folds between the endothelial cells. TEM demonstrated that these bodies contained many lipid particles, and numerous active microvilli were seen on the body surface. In the deeper subendothelial space, villi of each body interdigitated. From these results, it is postulated that the circulating leukocytes penetrate under the endothelium and take up the deposited lipids. Then, they return to the blood stream, containing lipid rich particles. The deposited lipids in the atherosclerotic lesion would be removed by this process. We named this phenomenon as "exo-tissuesis with lipid containers". While lipids are believed to be removed from the atherosclerotic lesion by HDL, lecithin cholesterol acyltransferase and others at the molecular level, we suggest that lipid containers play important roles in the regression and prevention of atherosclerosis on a major scale-cellular and tissue level.
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PMID:Studies on regression of atherosclerosis--role of lipid containers. 627 37


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